The influence of non-beta-blocking drugs on the lipid profile: are diuretics outclassed as initial therapy for hypertension?

Abstract

Diuretic drugs, when used in the treatment of hypertension, raise the blood concentrations of total cholesterol and low-density or very low-density lipoprotein cholesterol. Triglycerides often increase as well. Thiazide, phthalimidine, loop, potassium-sparing, and methylindoline drugs produce a similar effect. Only indapamide, a methylindoline agent with vasodilator activity, has been free of adverse lipid effects. It remains unclear whether it is the low dose of indapamide or some other quality that frees it of this effect. In long-term diuretic therapy, total cholesterol returns to, or below, baseline values, suggesting that the lipid elevations are transitory. However, in studies with adequate control groups, total cholesterol declines below baseline valves in control subjects such that an adverse differential in lipid values persists in long-term treatment. Selective alpha-1-adrenoceptor-blocking drugs cause no change or favorable alterations in lipid concentrations in short-term and long-term (1 year) treatment. Among all antihypertensive drugs, this class of agents, and especially prazosin, has produced the most consistently salutary lipid and metabolic effects. Although less well examined, guanabenz, clonidine, guanfacine, and diltiazem have been associated with favorable lipid changes. Captopril and nifedipine have caused no change in lipid-lipoprotein values in limited investigations. These agents are preferable to diuretics and certain beta blockers with respect to short-term effects on lipids and lipoproteins. Their ultimate superiority as monotherapy depends on whether they lower blood pressure equally well. Lowering of the probability of coronary heart disease in hypertensive patients depends as much on blood pressure control as on lipid effects.(ABSTRACT TRUNCATED AT 250 WORDS)